Suppression of a DNA polymerase δ mutation by the absence of the high mobility group protein Hmo1 in Saccharomyces cerevisiae
Suppression of a DNA polymerase δ mutation by the absence of the high mobility group protein Hmo1 in Saccharomyces cerevisiae
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DOI：
10.1007/s00294-009-0229-y
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发表时间：
2009-04-01
期刊：
影响因子：
2.5
通讯作者：
Livingston, Dennis M.
中科院分区：
文献类型：
--
作者：
Kim, Haeyoung;Livingston, Dennis M.
在限制性温度下，编码高迁移率族蛋白Hmo1的基因的缺失抑制了DNA pol Delta突变pol3-14的生长迟缓。Pol3-14突变细胞经历细胞周期停滞，而hmo1 Delta减轻了允许双突变继续分裂的停滞。细胞周期控制的旁路随着突变率的增加而发生。Pol3-14和hmo1 Delta都是突变子，它们的结合引发了CAN1突变的协同作用。RAD18控制DNA修复通路的分支，其缺失也抑制pol3突变。比较pol3-14的hmo1 Delta和rad18 Delta抑制表明，虽然两者都需要RAD52介导的修复，但它们的抑制是独立的，因为两者都可以在对方存在的情况下抑制。我们得出结论，hmo1 Delta抑制pol3-14的发生是通过一种机制，即破坏对DNA完整性的正常控制，损伤流入RAD52介导的修复和容易出错的途径。
The deletion of the gene encoding the high mobility group protein Hmo1 suppresses the growth retardation of the DNA pol delta mutation, pol3-14, at the restrictive temperature. pol3-14 mutant cells undergo cell cycle arrest, and hmo1 Delta alleviates the arrest permitting continual division of the double mutant. Bypass of cell cycle control occurs with an increased rate of mutation. Both pol3-14 and hmo1 Delta are mutators and their combination provokes a synergistic rate of CAN1 mutations. RAD18 controls branches of DNA repair pathways and its deletion also suppresses pol3 mutations. Comparing hmo1 Delta and rad18 Delta suppression of pol3-14 shows that while both require the presence of RAD52-mediated repair, their suppression is independent in that both can suppress in the presence of the other. We conclude that hmo1 Delta suppression of pol3-14 occurs by a mechanism whereby normal controls on DNA integrity are breached and lesions flow into RAD52-mediated repair and error-prone pathways.